ミトゲンと腫瘍遺伝子は,特定の電圧誘導イオンチャネルの誘導をブロックすることができます
Science (New York, N.Y.)
|May 1, 1987
まとめ
筋肉細胞の成長停止は,電圧誘導カルシウム (Ca2+) とナトリウム (Na+) 経路の発達に必要である. 特定の腫瘍遺伝子は,このチャネル発現を遅らせたり抑制したりして,筋肉の電気生理学に影響を与えます.
科学分野:
- 細胞および分子生物学
- 神経科学は神経科学である.
- 筋肉生理学 筋肉生理学
背景:
- 筋肉細胞における電圧誘導イオンチャネルの発達メカニズムは,ほとんど不明のままである.
- 筋肉特異的な遺伝子発現は,典型的にはミトゲン離脱と成長停止によって誘発されます.
研究 の 目的:
- 筋肉細胞における電圧誘導イオンチャネル発現がミトゲン離脱と成長停止に依存しているかどうかを調査する.
- 筋肉細胞の分化過程におけるイオンチャネルオントゲニスを調節する細胞腫瘍遺伝子の役割を決定する.
主な方法:
- 実験のためにBC3H1筋細胞系を利用した.
- 機能的なイオンチャネルを検出するために,パッチクランプ技術を使用しました.
- 様々な腫瘍遺伝子の発現ベクトル (v-erbB,c-myc,Val12 c-H-ras) を持つ感染したBC3H1細胞.
主要な成果:
- 差別化されたBC3H1ミオサイトは,ミトゲン離脱から約5日後に現れる,機能的なCa2+とNa+チャネルを示した.
- 腫瘍遺伝子のv-erbBとc-mycが個別に遅れたが,Ca2+とNa+チャネルの出現を防ぐことはできなかった.
- Val12 c-H-rasまたはc-myc/v-erbB結合トランスフェクションは4週間以上,機能的なCa2+とNa+チャネル形成を抑制しました.
- カリウムチャネルは,ミトゲン媒介または腫瘍遺伝子の発現によって影響を受けませんでした.
結論:
- ミトゲンの撤退と成長停止は,筋肉細胞における機能的なCa2+とNa+チャネルの誘導に不可欠です.
- 特定の腫瘍遺伝子は,特にRasとMycを含む組み合わせは,電圧ゲートイオンチャネル開発を大幅に抑制することができます.
- イオンチャネル誘導に対する腫瘍遺伝子の媒介による効果は,筋肉細胞の分化に対するミトジェニック条件の抑制的な影響を反映しています.
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